1. Department of Otolaryngology and Center for Molecular Physiology of the Brain, University of Goettingen, 37099 Goettingen, Germany
2. INSERM U583–INM, BP 74103 and CRIC, University of Montpellier, 34091 Montpellier Cedex 5, France
3. Department of Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology, 39118 Magdeburg, Germany
4. Department of NanoBiophotonics, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, D-37077 Goettingen, Germany
5. Present address: Department of Neuroanatomy, Max Planck Institute for Brain Research, 60528 Frankfurt/M, Germany

Correspondence to: Tobias Moser¹ Correspondence and requests for materials should be addressed to T.M. (Email: tmoser@gwdg.de).

Abstract

Hearing relies on faithful synaptic transmission at the ribbon synapse of cochlear inner hair cells (IHCs)^{1, 2, 3}. At present, the function of presynaptic ribbons at these synapses is still largely unknown^{1, 4}. Here we show that anchoring of IHC ribbons is impaired in mouse mutants for the presynaptic scaffolding protein Bassoon. The lack of active-zone-anchored synaptic ribbons reduced the presynaptic readily releasable vesicle pool, and impaired synchronous auditory signalling as revealed by recordings of exocytic IHC capacitance changes and sound-evoked activation of spiral ganglion neurons. Both exocytosis of the hair cell releasable vesicle pool and the number of synchronously activated spiral ganglion neurons co-varied with the number of anchored ribbons during development. Interestingly, ribbon-deficient IHCs were still capable of sustained exocytosis with normal Ca²⁺-dependence. Endocytic membrane retrieval was intact, but an accumulation of tubular and cisternal membrane profiles was observed in ribbon-deficient IHCs. We conclude that ribbon-dependent synchronous release of multiple vesicles at the hair cell afferent synapse is essential for normal hearing.

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